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The expression of FBXW7 was mediated by miR-27a by directly binding to the 3'-untranslated region (3'-UTR) of FBXW7 in HSC3 cells. MiR-27a reversed partial roles of FBXW7 on the proliferation and invasion in OSCC cells. CONCLUSIONS FBXW7 was mediated by miR-27a and could inhibit the proliferation through the PI3K/AKT pathway and invasion-mediated EMT in OSCC cell line. The newly identified miR-27a/FBXW7/PI3K/AKT axis provides novel insights into the pathogenesis of osCC.OBJECTIVE To detect the expression of long intergenic non-coding ribonucleic acid (LINC) 01535 in esophageal squamous cell cancer (ESCC) tissues and cells, and to investigate the influences of LINC01535 on the proliferation and apoptosis of ESCC cells and the possible mechanism. PATIENTS AND METHODS Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the relative expression of LINC01535 in 43 cases of ESCC tissues and human esophageal cancer cells (KYSE30, EC9706, TE-13, and Ecal09) compared with human esophageal mucosal epithelial cells (HET-1A). The esophageal cancer cells with the highest expression were selected and transfected with small interfering RNA (si)-LINC01535 (experimental group) or si-negative control (NC) (control group). The interference efficiency was measured via qRT-PCR assay. Regulatory effects of LINC01535 on cell proliferative capacity was examined through colony formation assay and cell proliferation assay [Cell Counting Kit-8 (CCK-8)]. Cell cycle and egulating the JAK/STAT3 signaling pathway. Our findings provide new directions for the diagnosis and treatment of esophageal cancer.OBJECTIVE The aim of this study was to explore the expression of long non-coding ribonucleic acid (lncRNA) nuclear receptor subfamily 2 group F member 1-antisense RNA 1 (NR2F1-AS1) in esophageal squamous cell carcinoma (ESCC) tissues and cells and to investigate its effects on ESCC proliferation and metastasis. PATIENTS AND METHODS The expression level of NR2F1-AS1 in 51 pairs of ESCC tissues and corresponding adjacent tissues was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Meanwhile, NR2F1-AS1 expression in ESCC cells was measured via qRT-PCR as well. Subsequently, specific interference sequences of NR2F1-AS1 were designed, synthesized, and transiently transfected into ESCC cells. 48 h later, qRT-PCR assay was performed to detect the interference efficiency. The effects of small interfering (si)-NR2F1-AS1 on the proliferation of ESCC cells were determined through cell counting kit-8 (CCK-8) and colony formation assay. Wound healing and transwell assays were conducted igh expression of NR2F1-AS1 promoted the proliferation and metastasis of ESCC cells by modulating EMT.OBJECTIVE In recent years, circular RNAs (circRNAs) and microRNAs (miRNAs) have been shown to be related to the development of esophageal squamous cell carcinoma (ESCC). However, their functional mechanisms remain to be investigated. Herein, we focus our research on the functions and mechanisms of circCNOT6L and miR-384 in ESCC. MATERIALS AND METHODS The levels of circCNOT6L, miR-384, and fibronectin 1 (FN1) were determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). RNase R was used to investigate circCNOT6L stabilization. Cell proliferation and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Western blot assay was employed to analyze the protein levels of FN1, proliferation-related genes, and iron metabolism-related genes. In addition, the interaction between miR-384 and circCNOT6L or FN1 was predicted by starBase3.0 and confirmed by the Dual-Luciferase reporter assay. Mouse xenograft was carried out to measure the effect of circCNOT6L on tumor growth in vivo. RESULTS CircCNOT6L and FN1 levels were upregulated, and miR-384 level was downregulated in ESCC tissues/cells. CircCNOT6L knockdown attenuated ESCC cell proliferation and iron metabolism disorder, as well as accelerated apoptosis. Notably, circCNOT6L targeted miR-384, and miR-384 targeted FN1. MiR-384 depletion and FN1 upregulation weakened the effects of circCNOT6L knockdown and miR-384 overexpression on ESCC cell progression, respectively. Besides, circCNOT6L knockdown inhibited tumor growth in vivo. CONCLUSIONS Our results demonstrated that circCNOT6L positively regulated the development of ESCC cells via modulating miR-384/FN1 axis. Our findings provided a theoretical basis for the therapy of ESCC patients.OBJECTIVE The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1). PATIENTS AND METHODS Expression levels of miR-129-5p and HMGB1 in gastric cancer tissues (n=25) and adjacent normal tissues were measured via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The regulatory effect of miR-129-5p on the proliferation of gastric cancer MGC-803 and SGC7901 cells was determined through Cell Counting Kit-8 (CCK-8) assay. Flow cytometry was employed to analyze the apoptosis rate of gastric cancer cells. To further discover the mechanism of miR-129-5p in regulating malignant behaviors of gastric cancer cells, the miRDB database was employed to predict the binding targets of miR-129-5p. Finally, binding sites of HMGB1 3'-untranslated region (3'-UTR) to miR-129-5p were discovered. Subsequently, HMGB1 wild-type or mutant 3'ed significantly (p less then 0.001). HMGB1 overexpression overtly reversed the inhibitory effect of miR-129-5p on the proliferation of gastric cancer cells (p less then 0.05). All these results demonstrated that the miR-129-5p/HMGB1 axis played a key role in regulating the growth of gastric cancer cells. [https://www.selleckchem.com/products/at13387.html Onalespib mw] CONCLUSIONS MiR-129-5p suppresses the progression of gastric cancer through targeted inhibition on the expression of HMGB1.OBJECTIVE As the fourth most common malignant tumor with high mortality rate, gastric cancer (GC) seriously threatens people's health and life quality worldwide. The aim of this study was to explore the functional role of long non-coding RNA (lncRNA) BCAR4 in GC. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was used to detect the expression level of lncRNA BCAR4 in GC cell lines and tissues. Subsequently, cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry were recruited to investigate the role of lncRNA BCAR4 in the proliferation and apoptosis of GC cells, respectively. Western blotting was used to detect the protein expression level of mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK) in GC. Besides, tumor formation assay was applied to examine the ability of lncRNA BCAR4 in vivo. RESULTS LncRNA BCAR4 was highly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay, and flow cytometry results indicated that up-regulated lncRNA BCAR4 significantly promoted cell proliferation and suppressed cell apoptosis in GC.